Journal of Molecular Medicine

, Volume 84, Issue 6, pp 469–477

Fibrin(ogen) and its fragments in the pathophysiology and treatment of myocardial infarction

  • Kai Zacharowski
  • Paula Zacharowski
  • Sonja Reingruber
  • Peter Petzelbauer
Review

DOI: 10.1007/s00109-006-0051-7

Cite this article as:
Zacharowski, K., Zacharowski, P., Reingruber, S. et al. J Mol Med (2006) 84: 469. doi:10.1007/s00109-006-0051-7

Abstract

The occlusion of a coronary artery leads to ischemia of the myocardium, while permanent occlusion results in cell death and myocardial dysfunction. Early restoration of blood flow is the only means to reduce or prevent myocardial necrosis, but—paradoxically—reperfusion itself contributes to injury of the heart. In animal models, this phenomenon is well described, and there are many different unrelated approaches to reduce reperfusion injury. In humans, however, pharmacological interventions have so far failed to reduce myocardial reperfusion injury. We summarize the pathogenesis of reperfusion injury, detailing the role of fibrin(ogen) and its derivatives. Moreover, we introduce a new concept for fibrin derivatives as potential targets for reperfusion therapy.

Keywords

15–42Fibrin fragmentsEndothelial cellVE-cadherinLeukocyte transmigrationMyocardial infarction and reperfusion injury

Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  • Kai Zacharowski
    • 1
  • Paula Zacharowski
    • 1
  • Sonja Reingruber
    • 2
  • Peter Petzelbauer
    • 3
  1. 1.Molecular Cardioprotection and Inflammation Group, Department of AnesthesiaUniversity Hospital of DüsseldorfDüsseldorfGermany
  2. 2.Fibrex Medical Research and DevelopmentWienAustria
  3. 3.Department of General DermatologyMedical UniversityWienAustria